2009
DOI: 10.1007/s00281-009-0168-1
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Immune cell-mediated liver injury

Abstract: Liver diseases represent an important cause of morbidity and mortality in the world. Death of hepatocytes and other hepatic cell types is a characteristic feature of several forms of liver injury such as cholestasis, viral hepatitis, drug-or toxin-induced injury, and alcoholinduced liver damage.

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Cited by 23 publications
(17 citation statements)
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References 97 publications
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“…However, studies with an increased number of patients should be completed to evaluate this hypothesis. In addition, findings demonstrating that a strong and sustained CD4 + T cell-specific Th1 response during hepatotropic virus infections can result in clearance of viral infection (Corazza et al 2009) are consistent with our observation of IFN-γ over expression patients who resolved HBV infection (Fig. 4C).…”
Section: Discussionsupporting
confidence: 79%
See 1 more Smart Citation
“…However, studies with an increased number of patients should be completed to evaluate this hypothesis. In addition, findings demonstrating that a strong and sustained CD4 + T cell-specific Th1 response during hepatotropic virus infections can result in clearance of viral infection (Corazza et al 2009) are consistent with our observation of IFN-γ over expression patients who resolved HBV infection (Fig. 4C).…”
Section: Discussionsupporting
confidence: 79%
“…Additionally, it is accepted that liver damage is likely a result of the immune response to HBV infection (Racanelli & Rehermann 2006, Corazza et al 2009, Wang & Zhang 2009 OHB-infected Nahua natives to determine if cytokine expression levels distinguish OHB, genotype H-infected patients as a result of a coordinated immune response.…”
mentioning
confidence: 99%
“…Activation of the pro-inflammatory cytokine cascade such as TNFα is considered to play an important role in the pathophysiology and clinical outcome of severe liver injury [24], which has been confirmed with TNFα knockout or TNFα receptor p55 knockout mice [25,16]. This model was also studied for potential protection by sTNFRII-Fc and the two DNTNF biologics XENP1595 and XENP345 [26,27]. Most recently, TNFα-induced apoptosis was reported to be associated with Fas and FasL up-regulation.…”
Section: Discussionmentioning
confidence: 91%
“…Amounts of serum-soluble TNFR1 and TNFR2 were also found to be higher 8 h after BCG/LPS (sTNFR1: 5.5-fold, sTNFR2: 2-fold) than after D-GALN/LPS. These data reflect a different regulation and cell origin of solTNF and sTNFRs, which can be produced and released by many immune cells in the BCG/LPS mouse model, whereas in D-GALN/LPS-induced hepatitis, solTNF is predominantly secreted by Kupffer cells [37].…”
Section: Serum Levels Of Soltnf and Soluble Tnfr1 And Tnfr2 In Bcg/lpmentioning
confidence: 98%